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Fibrosis is an endpoint for multiple diseases and is driven by the excessive production and deposition of collagen and other extracellular matrix proteins in tissues and organs. The increase in tissue stiffness associated with fibrosis impacts the normal functioning of tissues such as the lung, kidney and liver. 

Aragen has a portfolio of in vivo fibrosis models and world class expertise to support clients in the development of anti-fibrotic therapeutic or prophylactic candidates. In hundreds of studies, over the course of more than a decade, we have evaluated the efficacy of test compounds spanning several modalities (small molecules, biologics, RNA therapeutics, exosomes etc.) on a variety of assay platforms, ultimately resulting in INDs for our clients. Our diet-induced, chemical-induced and surgical models of fibrosis, coupled with an extensive evaluation of disease biomarkers, as well as cellular and molecular mechanisms, can help drive research efforts towards finding novel therapies.

  • Liver Fibrosis
    • Streptozotocin (STZ)+high fat diet (HFD)-induced NASH
    • AMLN (Amylin Liver NASH) model in mice
    • Carbon tetrachloride (CCl4)-induced liver fibrosis
    • TAA-induced liver fibrosis
    • CDAHFD-induced NASH and liver fibrosis
    • Western diet+CCl4-induced NASH and liver fibrosis
  • Kidney Fibrosis
    • Unilateral ureteral obstruction (UUO)
    • 5/6 Nephrectomy
  • Lung Fibrosis
    • Bleomycin-induced idiopathic pulmonary fibrosis (IPF)
    • Silica-induced lung fibrosis
    • Scleroderma model/systemic sclerosis
  • Skin Fibrosis
    • Scleroderma model/systemic sclerosis
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